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Objectives: Mandibular resection for oral cancer is often necessary to achieve an adequate margin of tumor clearance. Mandibular resection has been associated with a poor health-related quality of life (HRQOL), particularly before free fibula flap to reconstruct the defect. The aim of this study was to evaluate health-related quality of life in patients who have had mandibular resections of oral cancer and reconstruction with free fibula flap. Study Designs: There were 115 consecutive patients between 2008 and 2011 who were treated by primary surgery for oral squamous cell carcinoma, 34 patients had a mandibular resection. HRQOL was assessed by means of the 14-item Oral Health Impact Profile (OHIP-14) and University of Washington Quality of Life (UW-QOL) questionnaires after 12 months postoperatively. Results: In the UW-QOL the best-scoring domain was mood, whereas the lowest scores were for chewing and saliva. In the OHIP-14 the lowest-scoring domain was social disability, followed by handicap, and psychological disability. Conclusions: Mandible reconstruction with free fibula flap would have significantly influenced on patients’quality of life and oral functions. The socio-cultural data show a fairly low level of education for the majority of patients. Key words:Health-related quality of life, free fibula flap, mandibulectomy, UW-QOL, OHIP-14.

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Oct4 and Sox2 are pluripotent stem cell factors but the interplay between them in tumorigenesis is unclear. The aim of the present study was to investigate the roles of Oct4 and Sox2 in the reprogramming of oral cancer stem cells. One or both Oct4 and Sox2 were overexpressed in immortalized oral epithelial (hTERT+-OME) cells by lentivirus transduction. In addition, Oct4 and Sox2 proteins in two oral squamous cell carcinoma cell (OSCC) lines (Cal27 and primary cultured OSCC from a T2N2M0 patient) were individually or combinedly knocked down by shRNA. The results showed that the doubly transduced (Oct4+Sox2+) cells could trigger neoplasms in immunodeficient mice after lentivirus transduction, but single transduced (Oct4+ or Sox2+) cells had no tumor formation ability. The knockdown Sox2low and knockdown Oct4lowSox2low cells resulted in decreased tumor size in the immunodeficient mice but the single knockdown Oct4low cancer cells acquired more aggressive xenografts. Our findings suggest that Oct4+Sox2+ cells may be reprogrammed cancer stem cells inducing oral carcinogenesis.

Objective: Accurate predictors for occult metastasis in cT1-2N0 tongue squamous cell carcinoma (SCC) remains scarce, the main goal in current study was to evaluate whether there is significant association between lingual lymph node (LLN) metastasis and occult lymph node metastasis as well as whether there is prognostic value of LLN metastasis in early stage tongue SCC. Methods: Patients with surgically treated primary cT1-2N0 tongue SCC were prospectively enrolled from January 2010 to December 2018. LLNs were dissected independently for pathologic analysis. The main study endpoints were locoregional control survival (LRC) and disease-specific survival (DSS). The Chi-square test and multivariate regression analysis were used to assess the predictors for occult metastasis. The Kaplan-Meier approach and Cox model were used to analyze the potential prognostic factors. Results: A total of 317 patients were enrolled for analysis. Eighty-eight patients had occult metastasis with a prevalence of 27.8%. LLNs presented in 89 patients, in which 43 patients had LLN metastasis. In the 43 patients with positive LLNs, 20 patients had occult metastasis, in 274 patients with negative LLNs or no LLNs, 68 patients had occult metastasis, the difference was significant (p = 0.012). Further multivariate regression analysis confirmed the independence of LLN metastasis in predicting the occult metastasis. In patients without LLNs, the 5-year LRC rate was 79%, in patients with negative LLNs, the 5-year LRC rate was 78%, in patients with positive LLNs, the 5-year LRC rate was 62%, the difference was significant (p = 0.024). In patients without LLNs, the 5-year DSS rate was 84%, in patients with negative LLNs, the 5-year DSS rate was 74%, in patients with positive LLNs, the 5-year DSS rate was 51%, the difference was significant (p < 0.001), further Cox model confirmed the independence of LLN metastasis in affecting the LRC and DSS. Conclusions: LLN metastasis is significantly associated with occult neck lymph node metastasis, and decrease the LRC and DSS in early stage tongue SCC.

The aim of this study was to explore the functions and associated mechanisms of long noncoding RNA LINC02487 in oral squamous cell carcinoma (OSCC). Methods:The relative expression levels of LINC02487 in OSCC cell lines and tissue samples were examined by RT-qPCR. Intracellular localization was determined using RNA fluorescence in situ hybridization. LINC02487 was cloned into the pCMV-puro vector and then introduced into OSCC cells using lentiviral transfection. Cell processes, such as proliferation, apoptosis, migration, and invasion, were subsequently examined. LINC02487-binding proteins were identified by ChIRP-MS and confirmed by RNA immunoprecipitation. Protein expression was determined by western blotting assay.Results: LINC02487 has been reported to be downregulated in OSCC. Here, we confirmed that the expression of LINC02487 was reduced in 6 OSCC cell lines compared with that in immortalized normal oral epithelial cells and in 50 OSCC samples compared with paired adjacent normal tissue in a Chinese population and that LINC02487 expression levels were associated with cancer metastasis. We further identified that LINC02487 was localized to the cytoplasm, aggregated around the nuclear membrane. Functional studies demonstrate that overexpression of LINC02487 significantly suppresses cell migration and invasion and also inhibits cell proliferation. For the mechanism, we reveal that LINC02487 directly binds to USP17, a deubiquitinating enzyme, and regulates cell migration and invasion through the USP17-SNAI1 axis in a process that involves epithelial-mesenchymal transition (EMT). Conclusion:Our results confirm that long noncoding RNA LINC02487 is downregulated in OSCC tissue samples and cell lines. We also find that LINC02487 acts as a tumor suppressor through the USP17-SNAI1 axis.

Background and purposeDysregulated miRNAs play an important role in many malignant tumors. However, elucidating the roles of miRNAs in cancer biology, especially in epithelial cancers, remains an ongoing process. In this study, we identified the differentially expressed miR-645 in the progressing of head and neck squamous cell carcinoma (HNSCC) and investigated its biological function.MethodsThe association between clinicopathological parameters and the expression levels of the candidated miRNAs were analyzed by using the Kaplan–Meier survival analysis. The cell growth, invasion and migration potential, and clone formation were observed to detect the functions of the miRNAs in HNSCC cells.ResultsIn the 34 HNSCC tissues with lymph node metastasis, the expression level of miR-645 was 0.54 ± 0.12, and the expression level was 0.22 ± 0.05 in the 28 tissues with non lymph node metastasis (p = 0.017). In patients with HNSCC, higher level of miR-645 expression significantly correlates with worse overall survival (p = 0.04). Ectopic expression of miR-645 promoted cell invasion and migration.ConclusionsmiR-645 play a key role in cell invasion and metastasis and their expression correlates with overall survival in the patients with HNSCC.

1'-Acetoxychavicol acetate (ACA), extracted from rhizomes of tropical ginger, possesses antitumor properties against a wide variety of malignancies. MicroRNAs have been found to act as oncogenes and as tumor suppressor genes in the development of cancer. The purpose of this study was to investigate the miRNA involved in the molecular mechanisms of ACA action on tumor inhibition. It was found that ACA significantly inhibited the growth of human head and neck squamous cell carcinoma cell line HN4 and induced cell apoptosis. Further studies indicated that ACA downregulated the expression of miR-23a in HN4 cells. Transfection with anti-miR-23a inhibited the proliferation of HN4 cells and induced cell apoptosis. In addition, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was confirmed to be the target of miR-23a. Taken together, our findings suggest that ACA might have anticancer effects against human head and neck cancer through downregulation of miR-23a, which can repress tumor suppressor PTEN.